Quantification of Interneuron Damage in a Mouse Model for Prenatal Alcohol Exposure

Prenatal alcohol exposure (PAE) can result in a range of mental disabilities and physical
defects. Because adults affected by PAE demonstrate increased susceptibility to alcohol
dependence, it was hypothesized that PAE leads to the loss of inhibitory GABAergic
interneurons in corticostriatal circuits that regulate reward perception. Offspring of mice that
experienced acute ethanol exposure on gestation day 7 (GD 7) were used as an animal model.
Intracranial self-stimulation studies showed a marked difference in threshold for non-exposed
controls and PAE mice during the first 15 minutes following morphine injection, but no
significant difference was shown with alcohol or cocaine. Immunohistochemistry against
parvalbumin was performed to visualize the GABAergic interneurons of the CNS in the nucleus
accumbens, medial prefrontal cortex, dorsal striatum, and medial septum. A preliminary count of
the interneurons in the nucleus accumbens showed no difference between control and PAE mice.
In the future, further quantification of GABAergic interneurons in all four regions of interest may
conclude that maternal ethanol ingestion on GD 7 causes significant damage to the normal
distribution of inhibitory interneurons in CNS structures associated with reward perception.

Creator

Park, SungAffiliation: Department of Biology
College of Arts and Sciences

Thesis advisor

Malanga, C. J.

Degree granting institution

University of North Carolina at Chapel Hill

Title

Quantification of Interneuron Damage in a Mouse Model for Prenatal Alcohol Exposure